COULD CANCER HIJACK YOUR CELLULAR POWERHOUSE??

COULD CANCER HIJACK YOUR CELLULAR POWERHOUSE??

It is a well known fact that one of the hallmarks of cancer is ‘defective cellular energy production‘ and evidence is mounting highlighting ‘Mitochondrial Dysfunction‘ is a precursor to chronic disease including cancer.

‘Metabolic studies in a variety of human cancers previously showed that loss of mitochondrial function preceded the appearance of malignancy and aerobic glycolysis.’

As the powerhouse of the cells, mitochondria are critical for every organism because of their role in producing energy while also controlling survival. The mitochondria of our cells are also involved in other cellular activities like signalling, cellular differentiation and control of cell cycle, including cell growth and apoptosis (programmed cell death). It therefore appears imperative to ensure our mitochondria remain switched on and functioning optimally.

Mitochondrial dysfunction in cancer cells: Numerous studies show that tumor mitochondria are structurally and functionally abnormal and incapable of generating normal levels of energy which is why one of the mechanisms in Chemotherapy drugs is to power up the mitochondria, with the aim of destroying cancer cells.

Important insight into cancer progression emerged last year when a group (Kashatus et al, 2015) demonstrated how cancer cells in fact hijack mitochondria to support enhanced anabolic respiration and promote tumor growth.

When cellular respiration falters and creates an inability for cells to properly utilize oxygen, the cells turn to fermenting glucose for their survival and become cancerous. Studies show that co-enzymes play a vital role in several of the mitochondrial processes within cells, it is vital for kick-starting mitochondria ATP production throughout the body and preventing chronic health conditions.

‘Evidence is reviewed supporting a general hypothesis that cancer is primarily a disease of energy metabolism. All of the major hallmarks of the disease can be linked to impaired mitochondrial function.‘